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Pancreatic Islets

Improving Vascularization in Pancreatic Islet Transplants

One of the approaches scientists have been exploring for the treatment of type 1 diabetes is pancreatic islet cell transplants. By introducing these cells into the body, they are often able to maintain better glycemic control and support insulin production. However, there are many challenges that come with this type of treatment. It is essential to protect transplanted islet cells from immune system attack while also promoting sustainability. Cells tend to lose function over time and poor vascularization is often a contributing factor.

In a recent study, scientists have found a way to improve vascularization and therefore function of transplanted human pancreatic islets in diabetic mice. In addition to encapsulating islet cells, they also included human umbilical cord perivascular mesenchymal stromal cells or HUCPVCs. The HUCPVCs had a positive effect on graft function and suppressed T cell responses. In both immunocompetent and immunodeficient diabetic mice, glycemic control was maintained for up to 16 weeks when cells were transplanted via a kidney capsule, and for up to six weeks or seven weeks respectively when administered via a hepatic portal route. Furthermore, with the addition of HUCPVCs to the transplanted islet mass, rejection was delayed and the graft showed some proregenerative properties.

These findings may improve the future of human islet allotransplantation as a viable option for long-term treatment of type 1 diabetes. Scientists are constantly exploring ways to reduce rejection and the need for prolonged immunosuppression while maintaining better glycemic control. This study opens doors for more advanced research on the use of HUCPVCs in islet transplantation as well as related therapies.

Diabetes Research Connection is committed to supporting research for type 1 diabetes by providing early-career scientists with essential funding to keep projects moving forward. Learn more about current studies and how to donate to these efforts by visiting https://diabetesresearchconnection.org.

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Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
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Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
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